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RBM10 Deficiency Promotes Anti-PD-1 Resistance in LUAD via STING Alternative Splicing-Driven CCL7 Signaling and

Weitong Gao¹, Ruqiong Wang¹, Bo An¹

¹Department of Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)

|June 22, 2026

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RNA-binding motif 10 (RBM10) deficiency in lung adenocarcinoma (LUAD) creates an immunosuppressive tumor microenvironment. Targeting the CCL7-CCR2 pathway can restore anti-PD-1 therapy efficacy in RBM10-deficient LUAD.

Area of Science:

Immunology
Molecular Biology
Oncology

Background:

Immune checkpoint inhibitors (ICIs) have improved lung adenocarcinoma (LUAD) treatment outcomes.
However, many LUAD patients show inadequate responses to ICIs.
The immunomodulatory roles of RNA-binding motif (RBM) proteins are not well understood.

Purpose of the Study:

To investigate the role of RBM10 in regulating the tumor immune microenvironment in LUAD.
To identify mechanisms by which RBM10 deficiency affects anti-tumor immunity and response to ICIs.
To explore therapeutic strategies to overcome ICI resistance in RBM10-deficient LUAD.

Main Methods:

In vivo and in vitro models of RBM10 deficiency.
Cytokine arrays, CLIP-seq, RIP, and proteomics.

Keywords:

RNA‐binding motif 10 alternative splicing immune checkpoint inhibitors mitochondrial transfer tumor‐associated macrophages

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Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes

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Analysis of macrophage polarization and recruitment.

Investigated STING splicing and CCL7 secretion.

Explored the role of the CCL7-CCR2 axis and mitochondrial transfer.

Main Results:

RBM10 deficiency promotes an immunosuppressive microenvironment in LUAD.
RBM10 loss impairs STING exon 3 exclusion, leading to increased CCL7 secretion.
CCL7 recruits and polarizes M2 tumor-associated macrophages (TAMs) via the CCR2 receptor.
A positive feedback loop involving M2 TAMs and mtDNA-cGAS-STING signaling sustains CCL7 production.
Targeting chemokines or the CCL7-CCR2 axis restores anti-PD-1 efficacy.

Conclusions:

RBM10 is a key immunoregulator in LUAD, controlling the STING-CCL7-CCR2 axis.
RBM10 deficiency drives immunosuppression and resistance to anti-PD-1 therapy.
Targeting the CCL7-CCR2 axis offers a promising strategy to enhance anti-PD-1 therapy in LUAD.